Our previous results demonstrated that the ischemic edema is associated with an increased release of 5-HT and kinetic changes in the properties of synaptosomal serotonin (S-2)-receptor binding sites. In another study we have also shown that either preischemic or postischemic treatment of gerbils with Gamma-hydroxybutyrate (GHB), an endogenous central nervous system depressant, reduces the formation of edema and stabilizes the 5-HT metabolism. To shed some more light on the pathomechanisms of edema formation, we investigated the preischemic GHB effect on S-2-receptor binding sites in the ischemic model of edema on gerbils subjected to 15 min bilateral carotid artery occlusion and release for 1 hr. These studies have shown that GHB given prior to the inducion of bilateral carotid artery occlusion in gerbils prevented the ischemically induced changes in S-2-receptor binding sites using 3H-ketanserin as ligand (which labels specifically S-2-receptor sites). Thus, the capability of GHB to reduce the formation of ischemic edema and stablize the 5-HT metabolism (observed in previous studies), as well as to prevent ischemic changes in the kinetic properties of S-2-receptor binding sites, reinforces the contention of GHB effect of 5-HT metabolic pathway.